Evidence map›Paper›PMID 39409173›Full record

ArticleInternational journal of molecular sciences2024

B-Cell Maturation Antigen (BCMA) as a Biomarker and Potential Treatment Target in Systemic Lupus Erythematosus.

Jonas Martin, Qingyu Cheng, Sarah A Laurent, Franziska S Thaler, Anne Elisabeth Beenken, Edgar Meinl, Gerhard Krönke, Falk Hiepe, Tobias Alexander

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 2 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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  7. B-cell-targeting therapies in podocytopathies.Pediatric nephrology (Berlin, Germany) · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Jonas MartinDepartment of Rheumatology and Clinical Immunology, Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany.ORCID 0009-0008-2173-2397
Qingyu ChengDepartment of Rheumatology and Clinical Immunology, Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany.
Sarah A LaurentInstitute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians-Universität München, 80336 Munich, Germany.
Franziska S ThalerInstitute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians-Universität München, 80336 Munich, Germany.
Anne Elisabeth BeenkenDepartment of Rheumatology and Clinical Immunology, Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany.
Edgar MeinlInstitute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians-Universität München, 80336 Munich, Germany.ORCID 0000-0002-2570-6785
Gerhard KrönkeDepartment of Rheumatology and Clinical Immunology, Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany.
Falk HiepeDepartment of Rheumatology and Clinical Immunology, Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany.
Tobias AlexanderDepartment of Rheumatology and Clinical Immunology, Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany.ORCID 0000-0003-1193-0097

Funding

Deutsche Forschungsgemeinschaft SFB-TR128 TP B08 and TR130 TP15
6 · The paper itself

Abstract

The BAFF-APRIL system is crucial for the pathogenesis of systemic lupus erythematosus (SLE) by promoting B cell survival, differentiation and the maintenance of humoral autoimmunity. Here, we investigated the relationship of BCMA expression on B cell subsets with its ligands BAFF and APRIL, together with soluble BCMA, and with clinical and serologic variables in a cohort of 100 SLE patients (86 under conventional and 14 under belimumab therapy) and 30 healthy controls (HCs) using multicolor flow cytometry and ELISA. We found that BCMA expression in SLE patients was significantly increased on all B cell subsets compared to HCs, with all examined components of the BAFF-APRIL system being upregulated. BCMA expression was significantly increased on switched and unswitched memory B cells compared to naïve B cells, both in HCs and SLE. BCMA expression on B cells correlated with plasmablast frequencies, serum anti-dsDNA antibodies and complement consumption, while soluble BCMA correlated with plasmablast frequency, highlighting its potential as a clinical biomarker. Belimumab treatment significantly reduced BCMA expression on most B cell subsets and soluble TACI and contributed to the inhibition of almost the entire BAFF-APRIL system and restoration of B cell homeostasis. These results provide insights into the complex dysregulation of the BAFF-APRIL system in SLE and highlight the therapeutic potential of targeting its components, particularly BCMA, in addition to its use as a biomarker for disease activity.

Indexed as

Antibodies, Monoclonal, HumanizedB-Cell Activating FactorB-Cell Maturation AntigenBiomarkersLupus Erythematosus, SystemicTumor Necrosis Factor Ligand Superfamily Member 13AdultAntibodies, AntinuclearB-LymphocytesB-Lymphocyte SubsetsCase-Control StudiesFemaleHumansMaleMiddle AgedAntibodies, AntinuclearAntibodies, Monoclonal, HumanizedB-Cell Activating FactorB-Cell Maturation AntigenbelimumabBiomarkersTNFRSF17 protein, humanTNFSF13B protein, humanTNFSF13 protein, humanTumor Necrosis Factor Ligand Superfamily Member 13BAFFB cellsBCMAlupusplasma cellsSLETACI

Identifiers

PMID39409173
PMCPMC11476889

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.